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RJ, 51, PRESENTS TO THE ED complaining of the worst headache of her life, nausea, and photophobia. Computed tomography (CT) of the brain shows blood in the subarach-noid space. The blood resulted from a ruptured aneurysm.

Aneurysmal subarachnoid hemorrhage (aSAH) is frequently deadly, and outcomes are poor for many survivors. The American Heart Association and American Stroke Association have updated their guidelines on the manage-ment of patients with aSAH. This article reviews the current guide-lines, which cover incidence, prevalence, treatment, and preven-tion of complications associated with aSAH.

Pressure on a weakened wallCerebral aneurysms develop when an artery wall becomes thin and weak. When a thinned arterial wall ruptures, blood from the ruptured aneurysm accumulates in the sub-arachnoid space.1

Many factors are known to con-tribute to aneurysm formation, in-cluding smoking, hypertension, and connective tissue disorders.1 One process recently recognized in aneu-rysm formation and growth is in-flammation. Use of statin drugs and calcium channel blockers may inhibit this process, but research is needed to confirm that these drugs are benefi-cial for aSAH prevention.2

Various patient characteristics affect the probability of aneurysm

rupture. Older adults, women, and people of Black or Hispanic ethnicity have higher rates of aSAH.2,3 (For details, see Risk f actors for aSAH.)

Patient and aneurysm character-istics can interact to increase the risk of rupture. For example, the risk of aSAH increases when the aneurysm is causing symptoms, such as abnormal extraocular move-ments associated with deficits in cranial nerves III, IV, and VI.1

Size matters too: In general, an-eurysms that are likely to bleed are larger than 7 mm. In hypertensive patients who smoke, however, aneu-rysms that hemorrhage tend to be smaller than those in nonsmoking patients who are hypertensive or

Aneurysmal subarachnoid hemorrhage

By Wendi Rank, MSN, RN, CNRN, CRNP

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those in normotensive patients who smoke.2

An estimated 14.5 per 100,000 people are diagnosed with aSAH, but the actual figure is undoubtedly higher because 12% to 15% of pa-tients die before they can get medical care. The statistics on patients who experience aSAH are grim: About 32% of those who reach the hospital die. Of all patients diagnosed with aSAH in a hospital setting who survive the initial hemorrhage, 50% to 66% suffer complications.1,3

Research has identified several fac-tors contributing to aSAH morbidity and mortality. (See Predictors of poor patient outcomes.) In addition, the likelihood of survival after aSAH may be affected by sex and race. Some studies suggest that men are more likely to survive than women. Sur-vival rates are also higher for Whites than for Blacks, American Indians, Native Alaskans, Asians, and Pacific Islanders.2

To prevent aSAH, hypertension should be treated, and patients should refrain from smoking and excessive alcohol use. Diets with high vegetable content should be encour-aged because one study showed aSAH decreased as vegetable intake increased.2,4 In patients with a known, unruptured aneurysm, the healthcare provider will consider the shape and hemodynamics of the

aneurysm when planning treatment. Patients who have a family or per-sonal history of aSAH can be moni-tored for new aneurysms or blood flow within a treated aneurysm. Screening studies for these patients should be noninvasive to reduce the risk of complications.2,5

The setting in which a patient with aSAH receives treatment has also been shown to impact patient outcome. Large teaching institutions and hospitals with endovascular ca-pabilities are associated with lower morbidity and mortality. This seems to be especially true the more fre-quently a facility employs neuro-interventional procedures, such as endovascular coil embolization for cerebral aneurysms. Patients tend to have better outcomes in hospitals that treat more than 35 patients with aSAH per year.2

Patients whose presentation sug-gests aSAH should be diagnosed as quickly as possible to improve the chances of survival and a good re-covery. For optimal care, they should be admitted to a facility with neuro-interventional capabilities and a neurologic ICU, even if they must be transferred.2

Recognizing signs and symptomsThe headache of aSAH typically be-gins abruptly. Like 80% of patients experiencing aSAH, RJ described her headache as the worst of her life. However, some patients (10% to 43%) have a less intense headache, known as a sentinel headache, before aneurysm rupture. This type of head-ache is associated with an increased risk that the aneurysm will rebleed in the absence of treatment.2

Meningeal signs and symptoms, which develop when the hemor-rhaged blood irritates the meninges, include photophobia (light sensitiv-ity), blurred vision, nausea, vomiting, nuchal rigidity (stiff neck), and pain in the neck and back.1 Other signs and symptoms include altered level of consciousness (LOC), cranial

nerve deficits, and focal neurologic deficits, such as right hemiparesis.

Patients may also experience vital sign changes, such as hypertension. Seizures, a sign of aSAH in 20% of patients, usually occur in the first 24 hours.1,2 Immediately placing patients on antiepileptic drugs (AEDs) and initiating seizure pre-cautions is standard procedure.

Symptomatology is an important issue in aSAH diagnosis because outcomes are negatively affected if the diagnosis is delayed or missed. Approximately 12% of aSAH pa-tients aren’t diagnosed correctly.2 Failure to perform a noncontrast head CT, the gold standard for diagnosing aSAH, is a common reason for a missed diagnosis.

Diagnostic testingNoncontrast CT of the brain has nearly 100% sensitivity for diagnosing aSAH in the first 72 hours after rupture. Lumbar puncture may be performed if presenting signs and symptoms are consistent with aSAH but the CT fails to show hemorrhage. Computed tomography angiography (CTA) and magnetic resonance imaging (MRI) can also be used for some populations; for

Predictors of poor patient outcomes2

• significant acuity at presentation (the predominant predictor)

• aneurysm rebleeding• comorbidities• increased age• global cerebral edema at presen-

tation• presence of intraventricular and

intracerebral hemorrhage• symptomatic vasospasm• delayed cerebral infarction

(particularly more than one)• systemic complications, such as

fever, hyperglycemia, anemia, pneumonia, sepsis

• aneurysm-specific characteristics: larger size, anatomical locations that are difficult to treat (such as poste-rior circulation), irregular shape.

Risk factors for aSAH2,23

Modifiable• Smoking• Drug and alcohol abuse• Hypertension• Extremely low BMI.

Nonmodifiable• One or more first-degree family

members with cerebral aneurysm• Specific genetic syndromes, such

as autosomal dominant polycystic kidney disease and Ehlers-Danlos syndrome

• Family history of aneurysm• Personal history of unruptured

cerebral aneurysm• Family or personal history of aSAH



example, patients at risk for radiation overexposure.2

After aSAH is diagnosed, the an-eurysm needs to be located. If the patient may be a candidate for en-dovascular treatment, the surgeon must visualize the aneurysm’s precise shape. Cerebral digital subtraction angiography (DSA) is the most commonly used tool for locating the site of rupture.

In CTA, another option, a contrast medium is used with CT to create images of the cerebral arteries. However, using CTA alone to locate a ruptured aneurysm remains con-troversial. Research indicates that CTA may lack the sensitivity to identify aneurysms smaller than 3 mm. Based on current evidence, CTA may not provide as much information as DSA.2,5,6

After RJ’s aSAH is diagnosed via noncontrast CT, she has two- and three-dimensional DSA, which is more sensitive for identifying aneu-rysms than two-dimensional DSA alone.2 DSA shows that her aneu-rysm is located on her right posterior communicating artery (PCOM). (See Where to find cerebral aneurysms.)

Although RJ has just been diagnosed, she’s already received

Where to find cerebral aneurysms1

Most cerebral aneurysms form at the bifurcations and branches of the large arteries at the base of the brain, called the circle of Willis, which is located within the subarachnoid space. Arteries in the circle of Willis may be divided into anterior circulation (carotid portion) and posterior circulation (vertebrobasilar portion). The arteries most likely to develop aneurysms are as follows:

Anterior circulationAnterior communicating artery (ACOM)Middle cerebral artery (MCA)Anterior cerebral artery (ACA)Posterior communicating artery (PCOM)

Posterior circulationBasilar artery (BA)Vertebral artery (VA); not shown

Anterior communicating artery

Anterior cerebral artery

Middle cerebral artery

Posterior communicating artery

Circle of Willis

Posterior cerebral artery

Basilar artery

Aneurysm



radiation from a CT scan and DSA and she’s likely to undergo more cerebral radiation throughout her treatment course. Complications from receiving so much radiation, such as dermal erythema, alopecia, and cancer, are a significant threat.2,7 Her providers and the radiology staff closely monitor RJ’s radiation expo-sure and minimize the amount of radiation she receives by using non-radiation tests whenever possible and spacing tests requiring radiation apart.7

Grading aSAHAfter diagnosis, aSAH should be graded quickly to aid in predicting patient outcome and making treatment decisions. One frequently used system is the Hunt-Hess classification system, which grades the patient’s aSAH based on signs and symptoms.1,2 RJ is a Hunt-Hess Classification Grade II, which is associated with cranial nerve palsy, moderate-to-severe headache, and nuchal rigidity. (See Grading aSAH with the Hunt-Hess classification system for a complete description.)

While RJ awaits treatment, the nurse assesses her vital signs, performs neurologic assessments as prescribed, initiates seizure precau-tions according to facility policy, and closely monitors her. Standard nursing interventions include:• ensuring bed rest with head of bed elevated 30 degrees• initiating continuous cardiac monitoring

• documenting intake/output meticulously• providing prophylaxis for venous thromboembolism• ensuring a low level of external stimulation.1

Immediately report any changes in the patient’s condition. Acute compli-cations of aSAH, which are discussed in detail below, can develop before definitive treatment of the aneurysm is initiated.3

To prepare a patient for CT, CTA, or DSA, the nurse explains the proce-dure and tells the patient that he or she will need to lie still to optimize image quality. Iodinated contrast is used in CTA and DSA, so the nurse assesses for allergies, renal dysfunction, and metformin use before the procedure. Patients of childbearing potential should also be screened for pregnancy. The nurse explains that venous access is needed for contrast in CTA, and arterial access is used in DSA.

After the procedure, the nurse observes for signs and symptoms of contrast reactions, such as angio-edema or oliguria. For patients who undergo DSA, the arterial access site (usually the femoral artery) is closely monitored for active bleeding and expanding hematoma. The neurovas-cular status of the access extremity is also frequently assessed. The patient will be positioned supine, with the head of the bed flat and the affected leg immobilized, as prescribed, if

manual or mechanical compression was used to achieve hemostasis.1,3,8

It’s complicated, part I: Before treatmentThroughout diagnostic testing and treatment, the nurse must closely monitor the patient for complica-tions and intervene appropriately. Hydrocephalus develops in 15% to 87% of patients soon after aSAH because blood from the hemorrhage obstructs the subarachnoid villi and prevents cerebrospinal fluid (CSF) reabsorption.1,2

After her CT, RJ becomes lethargic and confused. Besides locating the aSAH, the CT revealed communicat-ing hydrocephalus. A ventriculos-tomy is performed for external ventricular drainage (EVD). EVD allows clinicians to monitor intra-cranial pressure (ICP) and control elevated ICP by periodically drain-ing CSF.

As an alternative to ventriculos-tomy, a lumbar drain can be placed. Although current evidence suggests patients with lumbar drains have less vasospasm than patients with EVD, caution is advised. The guide-lines note the risk of tissue shift and herniation after lumbar drain insertion in patients with severe aSAH. In some cases, lumbar drain placement results in brain herniation and death.2,3

Grading aSAH with the Hunt-Hess classification system1

Grade Signs and symptoms

I Asymptomatic or minor headache, slight nuchal rigidity

II Moderate-to-severe headache, nuchal rigidity, no neurologic deficit except cranial nerve deficits

III Minor focal deficit, lethargy or confusion

IV Moderate-to-severe hemiparesis, stupor

V Coma, decerebrate rigidity, moribund appearance

Risk factors for seizures after aSAH2,9

Early seizure• ruptured MCA aneurysm• aneurysm rebleeding• cerebral infarction• high-grade aSAH• large subarachnoid thrombus• intracerebral hemorrhage• patient history of hypertension

Late seizure• ruptured MCA aneurysm• cerebral infarction• intracerebral hematoma• previous seizure• refractory hypertension.



The nurse monitors RJ’s ICP and drains CSF as prescribed to manage ICP. The nurse assesses RJ for signs and symptoms of infection (such as fever and cloudy CSF) and aneurys-mal rebleeding and elevated ICP (such as sudden, severe headache, altered level of consciousness, new neurologic deficits, and fresh blood in the CSF).1

Early seizures, which develop in 6% to 26% of patients with aSAH, occur in the first 24 hours after aSAH.9 (See Risk factors for seizures after aSAH.) This is why initiation of AED therapy immediately after diag-nosis is standard practice. Although not well researched, it’s an accepted therapy because early seizures can compound neurologic injury, and rebleeding is a concern if the aneu-rysm hasn’t been repaired. Because serious adverse reactions are associ-ated with AEDs, closely monitor patient response and review lab values for therapeutic serum drug levels and signs of drug-related complications, such as agranulocy-tosis or thrombocytopenia. Assess for potential drug interactions.

The most serious acute complica-tion of aSAH is rebleeding, which is a risk until the aneurysm can be defini-tively treated. Patient morbidity and mortality is drastically increased when an aneurysm rebleeds.2

Almost half of aneurysms that rebleed do so within 6 hours of the initial bleed. The earlier an aneurysm rebleeds, the poorer the patient prog-nosis. A higher risk of rebleeding is associated with:• large aneurysms• poor neurologic condition• decreased LOC at time of rupture• history of sentinel headache• systolic BP over 160 mm Hg• a long delay before the aneurysm is obliterated.2

Several measures can be employed to prevent rebleeding until definitive treatment of the aneurysm is com-plete. RJ remains on bed rest with minimal external stimulation. Pre-venting hypertension is commonly

believed to reduce the risk of rebleed-ing. Research into exact BP limits and optimal medical therapy to maintain those limits is lacking, but the guide-lines note that keeping systolic BP below 160 mm Hg is “reasonable,” because higher pressures may be a risk factor for rebleeding.2 BP should be managed with a drug that can be easily titrated, such as nicardipine, and maintained at a level that’s suf-ficient to sustain cerebral perfusion pressure (CPP) and prevent acute ischemic stroke.1,2

An estimate of the adequacy of cerebral circulation, CPP is calcu-lated by subtracting ICP from mean arterial pressure. In healthy adults, a normal CPP is 70 to 100 mm Hg.1 Before treatment for aSAH, CPP should be kept within normal limits.

RJ’s ICP remains unstable despite her EVD. Because she couldn’t toler-ate lying flat prior to her DSA, defini-tive treatment was delayed, placing her at increased risk for rebleeding.

For patients whose definitive treatment is delayed, an antifibrinol-ytic such as aminocaproic acid or tranexamic acid may be prescribed to decrease the risk of rebleeding. Al-though not currently FDA-approved for this use, these drugs are consid-ered a reasonable precaution for up to 72 hours in cases of delayed treatment under the guidelines.2

Both drugs carry warnings regard-ing the increased incidence of certain neurologic complications when used for patients with aSAH.2,10,11 One study identified higher rates of hy-drocephalus possibly attributable to this therapy.2,10-13 However, because neurologic complications are associ-ated with aSAH and related diagnos-tic testing, the role of these drugs in development of these complications is unclear and research is ongoing.

Dilute aminocaproic acid as di-rected and avoid rapid infusion of either drug. Monitor the patient close-ly: Bradycardia has been observed in patients receiving aminocaproic acid, and both drugs can cause gastrointes-tinal upset and hypotension. Also

watch for signs and symptoms of systemic thrombosis and monitor lab values as prescribed.2,10,11

Surgery and moreThe only way to definitively treat a cerebral aneurysm is to occlude it from the healthy circulation. Two methods that achieve definitive treatment are surgical clipping and endovascular occlusion.1,2

• Surgical clipping is performed via open craniotomy. The surgeon places a clip at the base of the aneurysm, which stops blood from entering the aneurysm and prevents rebleeding. Surgical clipping is done under general anesthesia.1,3

• Endovascular occlusion, which is less invasive than surgical clipping, in-volves placing coils into the aneurysm via a catheter. This procedure can be performed with general anesthesia or moderate sedation/analgesia.1-3

The International Subarachnoid Aneurysm Trial (ISAT) is the only randomized, multicenter trial that has evaluated surgical clipping and endovascular coiling in patients with aSAH. It yielded valuable information that can assist the neurosurgical and endovascular teams in determining which treatment is in the patient’s best interest. Other trials that supple-ment the information gleaned from ISAT have been used to establish cur-rent treatment recommendations.2,14

Treatment decisions should in-volve collaboration between the neurosurgery team, the endovascular team, and the patient. All factors should be considered, including pa-tient acuity, comorbidities, aneurysm morphology, and aneurysm location.

When an aneurysm is amenable to both types of treatment, endovascular occlusion is usually considered. Results of ISAT indicated overall morbidity and mortality one year after aSAH were lower for patients undergoing endovascular treatment. Most studies agree that outcomes are better when aneurysms of the poste-rior cerebral circulation are treated endovascularly. Outcomes may also



be better in patients who are in vaso-spasm at the time of treatment and those with a “poor” Hunt-Hess grade. (The guidelines don’t specify a grade.)2,14 Endovascular occlusion may also be preferred if the aneurysm is at the apex of the basilar artery or if the patient is over age 70.2

However, endovascular occlusion has some shortcomings. To prevent rebleeding, ruptured aneurysms should be completely occluded if possible. Patients in ISAT who un-derwent endovascular coiling had an increased incidence of delayed rebleeding, and just 58% were totally occluded.

Coils also can compact over time, allowing blood to reenter the aneu-rysm. Stents used in conjunction with coiling and biologically active coils have been applied in attempts to achieve more durable occlusions. Some research suggests that stent assisted-procedures may increase the risk of complications, such as hemorrhage and thromboembolism, but more study is needed. Research into the long-term occlusion rates of biologically active coils is also needed.2,14

Patients with middle cerebral ar-tery (MCA) aneurysms have better outcomes with surgical clipping. Clipping may also be better for patients with intraparenchymal bleeding from the aSAH because the blood can be evacuated when the aneurysm is clipped. Early evacua-tion of intraparenchymal blood decreases morbidity and mortality.2

Research has been limited on anesthetic care during coiling and other aSAH-related endovascular treatments. The guidelines state that general anesthesia is useful for keeping the patient immobile and is applicable for certain patients under-going endovascular procedures.2,15

BP and blood glucose levels should be well-controlled during definitive treatment. Hypotension and hyper-glycemia during definitive treatment may both compound neurologic in-jury. Induced hypothermia to protect

the brain against ischemic injury isn’t well studied, but it may be appropri-ate for certain populations.2,16

Imaging should be done at the conclusion of any therapeutic inter-vention to confirm complete occlu-sion of the aneurysm. Noninvasive surveillance imaging studies are indicated for treated cerebral aneu-rysms. The time frame for this is at the discretion of the treatment team. Further treatment may be needed for aneurysms that continue to fill.2

Nursing care after treatmentRJ is treated with endovascular coil-ing. Before treatment, the nurse ex-plains to RJ and her family (with the patient’s permission) what to expect. The nurse reviews her lab test results and notifies the treating physician of any abnormalities. The nurse also notes her allergies and renal func-tion; even patients undergoing surgi-cal clipping may undergo angiogra-phy during surgery to confirm clip placement. Facility policy for stan-dard preoperative evaluations should be followed.1,3

Postprocedure, the nurse monitors the patient’s vital signs and neuro-logic status as prescribed, assessing for complications such as ischemia. The nurse also monitors her femoral access site and immobilizes her affected leg. Because a contrast me-dium was used, the nurse observes for signs of contrast-related compli-cations such as contrast-induced nephrotoxicity. Craniotomy patients should also be observed for bleeding or infection at the incision.1,3 Any signs or symptoms of complications must be reported immediately.

It’s complicated, part II: After treatmentA standard set of delayed complica-tions face aSAH patients. Delayed complications contribute to the high morbidity and mortality associated with aSAH.

Late seizures occur in 3% to 7% of patients. Long-term therapy with AEDs is a recommendation only

when the patient is at risk for late seizures; for example, because of previous seizures or refractory hypertension.2,3

Vasospasm is cerebral arterial constriction that can lead to ischemia and infarction. Although it can occur any time after rupture, vasospasm peaks at 7 to 10 days post-aSAH and doesn’t persist beyond 21 days.2

Signs and symptoms of vasospasm are related to cerebral ischemia and infarction. New focal neurologic deficits may develop and existing neurologic deficits may worsen. Altered LOC, particularly LOC that alternates in intensity, is another hallmark of vasospasm.1-3

Transcranial Doppler (TCD) ultra-sound can be used to assess blood velocity through the cerebral arter-ies. TCD studies are considered an acceptable tool to periodically screen patients with aSAH for asymptom-atic vasospasm.2

Delayed cerebral ischemia (DCI), a common complication of aSAH, is usually caused by vasospasm. Be-cause DCI and cerebral infarction are the end results of vasospasm, mul-tiple preventive therapies, screening and diagnostic studies, and treat-ments are indicated. Vasospasm, DCI, and cerebral infarction are the source of most morbidity and mortality in the weeks after aSAH.2

RJ’s neurosurgeon started her on oral nimodipine as soon as her aSAH was diagnosed. Nimodipine is a cal-cium channel blocker that decreases neurologic morbidity related to vaso-spasm. All aSAH patients should be started on nimodipine as soon as pos-sible and continue on it for 21 days. Nimodipine can cause hypotension, particularly in conjunction with other antihypertensives. Nimodipine me-tabolism can be affected by some AEDs, such as valproic acid, requir-ing dosage adjustments.2,17

Nimodipine is an oral drug. Take precautions to prevent inadvertent I.V. administration if the drug is withdrawn from the oral capsule for enteral administration. (See



“Nimodipine for Subarachnoid Hemorrhage: Patient Dies after I.V. Administration,” Medication Errors, page 72.)

RJ should be kept euvolemic to help prevent vasospasm. Her hemo-globin and hematocrit should be maintained as well. Although the ideal hemoglobin for patients with aSAH is unknown, those with higher hemoglobin have better outcomes. For patients with anemia, transfu-sions may be prescribed to improve cerebral oxygenation. In patients for whom DCI poses a significant threat, transfusion is a justifiable corrective measure.2,18-20

Chronic hydrocephalus develops in 9% to 48% of aSAH patients. No prophylactic therapy has been found to alter the rate of chronic hydroceph-alus. Weaning a patient from EVD over 24 hours doesn’t appear to re-duce the need for permanent surgical correction of chronic hydrocephalus.2

Patients with chronic hydrocepha-lus are treated with a permanent, internalized shunt. Postoperatively, monitor for standard surgical com-plications and observe the patient for signs of shunt failure, such as decreased LOC.1-3

The incidence of thrombosis, dis-seminated intravascular coagulation, disability, and death all increase in patients who develop heparin- induced thrombocytopenia (HIT). A hematologist should be consulted to aid in minimizing heparin use, be-cause it’s difficult to avoid in DSA and endovascular treatment. HIT and deep vein thrombosis (DVT) must be diagnosed early. No stan-dard screening procedures have been recommended, but screening for DVT hasn’t been shown to decrease the rate of pulmonary embolism.2

Managing vasospasmOn day 9 post-aSAH, RJ develops left upper extremity paresis. TCD studies indicate right MCA vasospasm. Recognizing that RJ has developed DCI as a result of vasospasm, her healthcare provider continues to

keep her euvolemic, but prescribes an I.V. vasopressor to induce hyper-tension and improve CPP. Patients with aSAH who develop DCI typi-cally improve with induced hyper-tension, but why is poorly under-stood. The guidelines don’t specify a means for inducing hypertension, but hypervolemia should be avoided because research has failed to sup-port its usefulness in DCI and vaso-spasm.1,2,21

RJ’s signs and symptoms fail to improve with induced hypertension. Preliminary research studies have indicated that perfusion imaging with CT or MRI may be better at lo-calizing ischemia than TCD studies.2 RJ’s perfusion CT confirms MCA vasospasm with corresponding ischemia.

RJ undergoes DSA, which also demonstrates vasospasm in the distal MCA branches. Because medical management has failed, the endovas-cular surgeon elects to use a balloon catheter to dilate the MCA. To open the distal arteries, a calcium channel blocker is infused intra-arterially. Although balloon angioplasty and vasodilator infusion haven’t been studied in large, randomized trials, they’ve been shown to be effective and are accepted treatments.2,22

RJ’s angiogram after her endovas-cular therapies shows her arteries have opened, and her signs and symptoms improve. She’ll still require frequent neurologic assess-ments, nimodipine, fluid manage-ment, and TCD studies.

Endovascular therapies work well to open the spastic arteries, but vaso-spasm can return once the treatment ends.2 RJ is closely monitored for medical complications, such as hyperglycemia, anemia, fever, sodium imbalance, decreased hemoglobin, and coagulopathies.

Other prioritiesFluid status and sodium level appear to impact the course of aSAH. Docu-menting intake and output closely and using central venous pressure

monitoring are acceptable applica-tions. Fluid status shouldn’t be ma-nipulated except in the presence of hypovolemia. Avoid hypotonic fluids in favor of colloids or crystalloids, as prescribed.2

Hyponatremia in aSAH may result from cerebral salt wasting or syn-drome of inappropriate antidiuretic hormone secretion. Symptomatic vasospasm and asymptomatic vaso-spasm identified by TCD have been linked to hyponatremia. In this set-ting, crystalloids, colloids, 3% sodium chloride, and hypertonic sodium chloride solutions have all been shown to be beneficial. Medical man-agement for hyponatremia can also include fludrocortisone and hydrocortisone.2

Hyperglycemia and hyperthermia should also be avoided. Normoglyce-mia in aSAH patients decreases the rate of poor outcomes. Correcting hyper- and hypoglycemia is a recom-mended strategy. Likewise, centrally triggered, noninfectious hyperthermia needs to be treated to prevent adverse effects on cognition and functionality. Any practical treatment is acceptable to employ in acute aSAH.2

The nurse monitors RJ’s vital signs, physical assessment findings, and lab test results as prescribed. The nurse also monitors for adverse effects of any treatments. For exam-ple, hydrocortisone used to correct sodium imbalance can cause hyper-glycemia, and blood transfusions or fluid administration can lead to fluid overload.1

Evaluation of cognition, behavior, and psychosocial issues is suggested once the patient is discharged.2 Many patients experience lingering memory, mood, and cognitive problems after treatment.

With judicious application of the recommendations, RJ’s outcome was optimized by the healthcare team. Discharged home with residual cog-nitive defects and a headache, she’ll follow up with the endovascular surgeon and a neurologist, and undergo outpatient rehabilitation. ■



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15. Lakhani S, Guha A, Nahser HC. Anaesthesia for endovascular management of cerebral aneurysms. Eur J Anaesthesiol. 2006;23(11):902-913.

16. Pasternak JJ, McGregor DG, Schroeder DR, et al; IHAST Investigators. Hyperglycemia in patients undergoing cerebral aneurysm surgery: its association with long-term gross neurologic and neuropsychological function. Mayo Clin Proc. 2008;83(4):406-417.

17. Drugs.com. Nimodipine prescribing information. http://www.drugs.com/pro/nimodipine.html.

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19. Naidech AM, Drescher J, Ault ML, Shaibani A, Batjer HH, Alberts MJ. Higher hemoglobin is associated with less cerebral infarction, poor outcome, and death after subarachnoid hemorrhage. Neurosurgery. 2006;59(4):775-779.

20. Naidech AM, Shaibani A, Garg RK, et al. Prospective, randomized trial of higher goal hemoglobin after subarachnoid hemorrhage. Neurocrit Care. 2010;13(3):313-320.

21. Dankbaar JW, Slooter AJ, Rinkel GJ, Schaaf IC. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a systematic review. Crit Care. 2010;14(1):R23.

22. Jun P, Ko NU, English JD, et al. Endovascular treatment of medically refractory cerebral vasospasm following aneurysmal subarachnoid hemorrhage. AJNR Am J Neuroradiol. 2010;31(10):1911-1916.

23. Singer RJ, Ogilvy CS, Rordorf G. Treatment of aneurysmal subarachnoid hemorrhage. UpToDate. 2013. http://www.uptodate.com.

Wendi Rank is a neurosurgical nurse practitioner in Southampton, Pa., and a board member of the Philadelphia chapter of the American Association of Neuroscience Nurses.

The author and planners have disclosed that they have no financial relationships related to this article.

DOI-10.1097/01.NURSE.0000428692.56721.36

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